Evidence map›Paper›PMID 25601927›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

miR-24, miR-30b, and miR-142-3p regulate phagocytosis in myeloid inflammatory cells.

Afsar Raza Naqvi, Jezrom B Fordham, Salvador Nares

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  12. Macrophage-enriched novel functional long noncoding RNAs LRRC75A-AS1 and GAPLINC regulate polarization and innate immune responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Afsar Raza NaqviDepartment of Periodontics, University of Illinois at Chicago, Chicago, IL 60612.
Jezrom B FordhamDepartment of Periodontics, University of Illinois at Chicago, Chicago, IL 60612.
Salvador NaresDepartment of Periodontics, University of Illinois at Chicago, Chicago, IL 60612 snares@uic.edu.ORCID http://orcid.org/0000-0002-2194-1374
University of Illinois Chicago · US

Funding

Functional Modulation of Myeloid Inflammatory Cells by miRNAR01DE021052 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI NARES, SALVADOR · 2011 to 2015
$1.9M
NIDCR NIH HHS DE021052NIDCR NIH HHS R01 DE021052
6 · The paper itself

Abstract

Micro-RNAs (miRNAs) are small noncoding RNAs that regulate various biological pathways. As their role in phagocytosis remains poorly understood, we investigated their impact on phagocytosis in myeloid inflammatory cells. Seven miRNAs (miR-24, -30b, -101, 142-3p, -652-3p, -652-5p, and -1275) that were differentially expressed during monocyte to macrophage (Mφ) and monocyte to dendritic cell (DC) differentiation were screened for their potential role in phagocytosis. Among these, overexpression of miR-24, miR-30b, and miR-142-3p in human monocyte-derived Mφ, DC, monocytes, and PBMCs significantly attenuate phagocytosis of Escherichia coli and Staphylococcus aureus, as well as the secretion of inflammatory mediators, including TNF-α, IL-6, and IL-12p40. miRNA-mediated changes in cytokine profiles were observed at transcriptional and/or posttranscriptional levels and importantly exhibit miRNA-specific impact. To examine the underlying mechanism, we monitored the expression of phagocytosis pathway-associated genes and identified several genes that were altered in Mφ and DC transfected with miR-24, miR-30b, and miR-142-3p mimics. Some of these genes with altered expression also harbor putative miRNA binding sites. We show that miR-142-3p directly regulates protein kinase Cα (PKCα), a key gene involved in phagocytosis. Interestingly, miR-142-3p and PKCα exhibit antagonistic expression during Mφ and DC differentiation. Short interfering RNA-mediated knockdown of PKCα in Mφ leads to reduced bacterial uptake, further highlighting the role of the gene in phagocytosis. Overall, these results demonstrate that miR-24, miR-30b, and miR-142-3p regulate phagocytosis and associated cytokine production in myeloid inflammatory cells through modulation of various genes involved in the pathway.

Indexed as

Blotting, WesternCytokinesFlow CytometryFluorescent Antibody TechniqueHumansInflammationMicroRNAsMyeloid CellsPhagocytosisReverse Transcriptase Polymerase Chain ReactionTransfectionCytokinesMicroRNAsMIRN142 microRNA, humanMIRN24 microRNA, humanMIRN30b microRNA, human

Identifiers

PMID25601927
PMCPMC4323870
OpenAlexW2168590981

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.